Targeting cancer stem cells as therapeutic approach in the treatment of colorectal cancer

Parizadeh, Seyed Mostafa; Jafarzadeh‐Esfehani, Reza; Hassanian, Seyed Mahdi; Vojdani, Samaneh; Ghandehari, Maryam; Ghazaghi, Anahita; Khazaei, Majid; Asgharzadeh, Fereshteh; Ferns, Gordon A.

doi:10.1016/j.biocel.2019.02.010

Cited by 36 publications

(32 citation statements)

References 79 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The colorectal cancer cells of HCT116 were digested and adjusted to 1 × 10 7 /mL, the counted cells in cell medium were mixed with matrigel with the ratio of 1:1 on ice, and then take 200 μL of the cell mixture seeded into the right axilla in Balb/c-nude mice with the cell numbers of 1 × 10 6 /mice. The xenograft mice were randomly divided into five groups (n = 12): model group, Capecitabine (Cap) 300 mg/kg group [28], Ls 75 mg/kg group, Ls 150 mg/kg group and Ls 300 mg/kg group, when the volume of the tumor growth to 100 mm 3 , which need about two weeks from the initial inoculation. The selected dosage of Ls was calculated from human to mice according to Chinese pharmacopoeia of 2010.…”

Section: Experimental Designmentioning

confidence: 99%

“…Colorectal cancer (CRC) is a common digestive tract malignancy, occurring in the colon and rectum. It is accounting for the second place in gastrointestinal cancer, and taking the third place in the incidence of cancer followed the lung cancer and gastric cancer, which generally observed after 40 years of age with a ratio of men and women as 2:1, serious threaten the human life and health in the worldwide [1][2][3][4]. Primary therapies applied to cure CRC are surgery, radiotherapy and conventional chemotherapy, despite progress in cancer control strategies of CRC, the patients survival rate have not been changed, especially for the patients with liver and lung metastases [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The mechanism and tumor inhibitory study of Lagopsis supine ethanol extract on colorectal cancer in nude mice

Wei

Wang

Xia

et al. 2019

BMC Complement Altern Med

View full text Add to dashboard Cite

Background: This study was aimed to determination the tumor inhibitory effect and explore the potential mechanisms of Lagopsis supine ethanol extract (Ls) on colorectal cancer. Methods: The cell growth inhibition experiment of Ls in colorectal cancer cell lines was determined by MTT method in the time course of 24, 48 and 72 h in four gradient drug concentrations. The protein expression levels of pSTAT3, pJAK2, STAT3, JAK2, Bcl-2 and caspase 3 were measured by Western blot method. The mRNA levels of the downstream genes of STAT3 were detected through semi-quantitative RT PCR. Sixty Balb/c-nude mice were xenograft with HCT116 colorectal cancer cells through subcutaneously. The xenografts were divided into five groups: model group, positive group (capecitabine 300 mg/kg) and three dosages of Ls treated groups (75, 150 and 300 mg/kg). Tumor size and tumor weight were calculated for evaluation the anti-tumor effects. H & E staining and immunohistochemical analysis were used to determine the histopathological changes and the levels of pSTAT3 and pJAK2 in the tumor tissues. Results: Ls exhibited a significant anti-proliferation effect in HCT116 and SW480 cells in vitro. The protein levels of pSTAT3, pJAK2 and Bcl-2, and the mRNA levels of Bcl-2 and Bak notably reduced with a dose-dependent manner. While the protein levels of caspase 3, and mRNA levels of Bax and caspase-3 remarkably increased in the gradient dosage of Ls in HCT116 cells. HCT116 in vivo xenografts experiment showed that the growth of the tumors significantly inhibited by Ls administration, which with no any significant body weight changes in each experiment group. The histopathology analysis displayed that Ls significantly reduced the inflammatory cells in tumor tissue. Furthermore, Ls also significantly down-regulate the protein levels of pSTAT3 and pJAK2 in the tumor tissues, compared with the model group. Conclusions: This work shows that Ls inhibited the cell proliferation of colorectal cancer in vitro and significantly reduced the tumor growth in HCT116 xenografts in vivo, which is probably related with the JAK/STAT signal pathway.

show abstract

Section: Experimental Designmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The mechanism and tumor inhibitory study of Lagopsis supine ethanol extract on colorectal cancer in nude mice

Wei

Wang

Xia

et al. 2019

BMC Complement Altern Med

View full text Add to dashboard Cite

show abstract

“…3 In recent decades, significant progress has been made in the prevention, diagnosis and treatment of CRC. 4,5 However, due to the complex pathogenesis of CRC, the 5-year survival rate of CRC was still very low. 6 Therefore, it is urgent to elucidate the molecular mechanism of CRC and explore new approaches to treat CRC.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Non-Coding RNA SNHG16 Activates USP22 Expression to Promote Colorectal Cancer Progression by Sponging miR-132-3p</p>

He¹,

Ma²,

Zhang³

et al. 2020

OTT

View full text Add to dashboard Cite

Background: Colorectal cancer (CRC) is the most common cause of cancer-related mortality in the world. Long non-coding RNAs (lncRNAs) are involved in the development of many cancers. However, studies on the effect of lncRNA small nucleolar RNA host gene 16 (SNHG16) on the proliferation, metastasis and apoptosis of CRC are still few. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine the expression levels of SNHG16, microRNA-132-3p (miR-132-3p) and ubiquitin specific peptidase 22 (USP22). The proliferation, apoptosis, migration and invasion of CRC cells were evaluated by the 3-(4,5-dimethyl-2 thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, flow cytometry and transwell assay, respectively. Dual-luciferase reporter assay was used to verify the interactions among SNHG16, miR-132-3p and USP22. Also, Western blot analysis was used to assess the protein levels of USP22 and metastasis-related markers. Moreover, mice xenograft models were used to determine the effect of SNHG16 on CRC tumor growth in vivo. Results: SNHG16 was highly expressed in CRC tissues and cells. Knockdown of SNHG16 reduced the proliferation, migration, invasion, and promoted the apoptosis of CRC cells. MiR-132-3p could interact with SNHG16, and its inhibitor recovered the suppression effect of silenced SNHG16 on CRC cell progression. Besides, USP22 was a target of miR-132-3p, and its overexpression restored the inhibition effect of miR-132-3p mimic on CRC cell progression. In addition, interference of SNHG16 reduced CRC tumor growth in vivo. Conclusion: LncRNA SNHG16 might act as an oncogene in CRC. The discovery of the SNHG16/miR-132-3p/USP22 pathway provided new thinking for the treatment of CRC.

show abstract

“…Since, phenotypic and functional properties of CSCs are regulated through a variety of extrinsic signaling pathways and intrinsic self-renewal factors [ 23 – 25 ], there is an urgent need to explore its details to provide specific targeted therapies for various cancers including ESCC. In the present study the correlation between expression pattern of MEIS1 and different stem cell markers including SALL4, OCT4, BMI-1, KLF4 and HIWI was investigated in ESCC patients and cell line to evaluate the potential correlation between MEIS1 and stemness state of the cells.…”

Section: Introductionmentioning

confidence: 99%

MEIS1 promotes expression of stem cell markers in esophageal squamous cell carcinoma

et al. 2020

View full text Add to dashboard Cite

Background: MEIS1 (Myeloid ecotropic viral integration site 1) as a homeobox (HOX) transcription factor plays regulatory roles in a variety of cellular processes including development, differentiation, survival, apoptosis and hematopoiesis, as well as stem cell regulation. Few studies have established pluripotency and self-renewal regulatory roles for MEIS1 in human esophageal squamous cell carcinoma (ESCC), and our aim in this study was to evaluate the functional correlation between MEIS1 and the stemness markers in ESCC patients and cell line KYSE-30. Methods: Expression pattern of MEIS1 and SALL4 gene expression was analyzed in different pathological features of ESCC patients. shRNA in retroviral vector was used for constantly silencing of MEIS1 mRNA in ESCC line (KYSE-30). Knockdown of MEIS1 gene and the expression pattern of selected stemness markers including SALL4, OCT4, BMI-1, HIWI, NANOG, PLK1, and KLF4 were evaluated using real-time PCR. Results: Significant correlations were observed between MEIS1 and stemness marker SALL4 in different early pathological features of ESCC including non-invaded tumors, and the tumors with primary stages of progression. Retroviral knockdown of MEIS1 in KYSE-30 cells caused a noteworthy underexpression of both MEIS1 and major involved markers in stemness state of the cells including SALL4, OCT4, BMI-1, HIWI and KLF4. Conclusions: The results highlight the important potential role of MEIS1 in modulating stemness properties of ESCCs and cells KYSE-30. These findings may confirm the linkage between MEIS1 and self-renewal capacity in ESCC and support probable oncogenic role for MEIS1 in the disease.

show abstract

Targeting cancer stem cells as therapeutic approach in the treatment of colorectal cancer

Cited by 36 publications

References 79 publications

The mechanism and tumor inhibitory study of Lagopsis supine ethanol extract on colorectal cancer in nude mice

The mechanism and tumor inhibitory study of Lagopsis supine ethanol extract on colorectal cancer in nude mice

<p>Long Non-Coding RNA SNHG16 Activates USP22 Expression to Promote Colorectal Cancer Progression by Sponging miR-132-3p</p>

MEIS1 promotes expression of stem cell markers in esophageal squamous cell carcinoma

Contact Info

Product

Resources

About